Current studies are directed to the mechanisms involved in cardiac failure as a consequence of septic and hemorrhagic shock. In addition the interrelationship between resucitation by crystalloid or colloid in the development of progressive respiratory failure termed the "wet-lung syndrome" is being explored. Using isolated heart preparations it has not been possible to demonstrate the presence of a myocardial depressive factor released either from the endotoxin-shocked animal or from the viscera after splanchnic arterial occlusion. Even when combined with a prolonged period of coronary hypoperfusion there was no evidence of significant myocardial depression. It has been possible to demonstrate decreased cardiac performance and response to volume loading in primates after six hours of shock and in isolated dog hearts. Specific studies of the pulmonary failure component have utilized both isolated perfused lungs and intact animals. Following the administration of endotoxin to swine, a marked increase in pulmonary vascular resistance occurs with secondary reduction of cardiac output. Both functional and anatomical determinations suggest that this is on a microembolic basis. Possible therapeutic approaches to the wet-lung syndrome have been explored including the use of positive end-expiratory pressure as an agent to mechanical ventilation which does result in improved oxygenation but fails to mobilize interstitial pulmonary edema. Further studies are in process to elucidate these mechanisms and to evaluate other forms of therapy.